大鼠肾上腺嗜铬细胞瘤细胞的神经型烟碱受体电流(英文)  

NEURONAL NICOTINIC ACETYLCHOLINE RECEPTOR CURRENTS IN CLONAL RAT PHEOCHROMOCYTOMA CELLS

作　　者：石丽君[1] 何永勇[2] 王春安[3] 

机构地区：[1]解放军北京军医学院生理学教研室,北京100071 [2]清华大学精仪系,北京100084 [3]第二军医大学生理学教研室,上海200433

出　　处：《神经解剖学杂志》2002年第1期27-31,共5页Chinese Journal of Neuroanatomy

摘　　要：本实验采用膜片箝技术观察了神经生长因子分化 5～ 10 d的大鼠肾上腺嗜铬细胞瘤 (PC12 )细胞上烟碱受体离子通道电流。在全细胞膜片箝条件下 ,当箝制电压为 -80 m V时 ,灌流乙酰胆碱 (ACh,3 0μmol/ L )诱发一内向电流 ,快速始发并衰减。此乙酰胆碱诱发电流 (IAch)随膜去极化和超级化而分别减小和增大 ,且被筒箭毒所阻断 ,可见此电流是由烟碱受体引起的。全细胞IACh呈较强的内向整流。其衰减相可被一双指数函数拟合 ,时间常数 (τ)分别在秒和分级。τf 对浓度的依赖性较τs强。 PC12细胞表面含有与交感神经元相似的烟碱受体 ,因此提供了一个交感神经元样的同源细胞株。Whole cell patch clamp technique was used to study nicotinic acetylcholine receptor ion channels (nAChR channels) in PC12 cells cultured in nerve growth factor (NGF) for 5～10 days. Perfusion of ACh (30 μmol/L) to the sympathetic like cell under the whole cell clamp produced an inward current at membrane potential of -80mV, which had a fast onset followed by a fast decay. This rapid ACh induced current(I ACh ) was accompanied by a large current fluctuation, i.e., the I Ach decreased or increased in amplitude by membrane depolarization or hyperpolarization, respectively, and was blocked by d tubocurarine. Thus this current must be induced by the nicotinic action of ACh. Furthermore, whole cell nAChR currents shows strong inwardly rectifying manner. The decay phase was well fitted by the sum of two exponential components with time constants (τ) in second and minute time scales, respectively. In addition, τ s was less concentration dependent than τ f. The clonal cell line PC12 provides a homogenous population of cells that contain on their surface nicotinic acetylcholine receptors that closely resemble those found on sympathetic neurons. It appears to be a good model system in studying regulation of a neuronal nicotinic ACh receptor.

关 键 词：膜片箝技术 离子通道电流 大鼠 肾上腺嗜铬细胞瘤细胞 神经型烟碱受体 

分 类 号：R730.2[医药卫生—肿瘤]